Claudia Robertson, MD-Cerebrovascular Dysfunction After Traumatic Brain Injury
Claudia Robertson, MD
Professor, Department of Neurosurgery
Baylor College of Medicine
The cerebrovasculature, which provide the brain with essential metabolic substrates, is often damaged after traumatic brain injury (TBI). Dysfunction ranges from vulnerability to secondary ischemic insults from impaired pressure autoregulation to severe global ischemia and death. Studies show that ischemia within 12 hours of injury correlates with mortality. Later, global ischemia appears as secondary, and may be preventable. Impaired pressure autoregulation may cause susceptibility to secondary insults for several days after injury. In experimental models, reduction in cerebral blood flow (CBF), accompanied by a decrease in tissue nitric oxide levels, can be ameliorated by giving L-arginine shortly after injury. Transgenic research models deficient in nitric oxide synthesis do not respond to L-arginine, confirming its role in early CBF reduction.
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